Food Animal - CNS Dz Flashcards
1
Q
List differential diagnoses for ruminants with an elevated white blood cell count in their CSF.
A
- Neutrophils: bacterial meningitis.
- Lymphocytes: viral encephalitis, listeriosis.
- Macrophages: trauma, polioencephalomyelitis.
- Eosinophils: parasite migration.
2
Q
List clinical signs of cerebral disease in ruminants.
A
- Excitement, mania.
- Seizures.
- Compulsive behaviour.
- Stupor.
- Coma.
- Abnormal vocalisation.
- Central blindness.
- Hyperaesthesia.
3
Q
What is the most common cause of symmetric cerebral disease in ruminants?
A
Metabolic abnormalities incl dehydration, acid-base abnormalities, electrolyte disturbances.
4
Q
Outline aetiologic agents of polioencephalomalacia (PEM) in ruminants.
A
- Thiamine deficiency.
- Sulphur toxicity.
- Lead toxicity.
- Salt toxicity.
5
Q
Describe the pathophysiology of thiamine deficiency in PEM of ruminants.
A
- Thiamine is produced by rumen microflora; production meets daily requirements; not stored.
- Thiamine essential for cerebral glucose metabolism; it is a co-enzyme of the pentose-phosphate pathway.
- Thiamine deficiency can be caused by rumen acidosis/disruption, thiamine inhibition or ingestion of plants containing thiaminases e.g. bracken fern, horsetail.
6
Q
Describe the pathophysiology of suphur toxicity in PEM of ruminants.
A
- Sulphur in the rumen is either assimilated into microbial protein or combines with H to form H2S.
- H2S is detoxified by the liver.
- Excess H2S prod –> overwhelms liver, or eructated and excess H2S inhaled.
- H2S inhibits cytochrome C oxidase –> no ATP –> neuronal swelling –> PEM.
- Source of S: feed intake limiters e.g. gypsum, by-products of corn, beet and sugar cane extraction e.g. molasses, water sources, S-accum plants incl rape, kale, turnips. Lamb’s quarters, Burning bush.
7
Q
Describe the pathophysiology of lead toxicity in PEM of ruminants.
A
- Lead has a profound effect on sulfhydryl-containing enzymes, the thiol content of erythrocytes, antioxidant defenses, and tissues rich in mitochondria –> cerebellar hemorrhage and edema associated w capillary damage.
- Industrial pollution from smelting.
- Junk piles: lead paint, gasoline and motor oil, insecticides, herbicides, lead batteries, shotgun pellets.
8
Q
Describe the pathophysiology of salt toxicity in PEM of ruminants.
A
- May be due to true salt poisoning e.g. ingestion of salt-licks, but usually due to water restriction.
- Alteration of cerebral energy metabolism –> dec pentose phosphate pathway activity –> dec ATP prod –> accum of Na –> oedematous swelling.
- Brain’s immediate response to hypertonic state is to lose water; rapid correction occurs through accum of electrolytes then idiogenic osmoles and water.
- RISK OF TX!! If you rapidly correct the hypertonic state cerebral oedema will occur due to the idiogenic osmoles.
9
Q
List clinical signs of PEM in ruminants.
A
- Depression/stupor.
- Central blindness.
- Convulsions.
- Head pressing.
- Aimless wandering.
- Inco-ordination.
- Ataxia.
- Muscle tremors.
- Opisthotonos.
- Dorsomedial strabismus.
- Nystagmus.
- Bruxism.
10
Q
Outline test results for diagnosis of PEM in ruminants.
A
- CSx and Hx.
- CBC/MBA/CSF cytology: rarely useful.
- CSF may have subjectively inc pressure on collection.
- Thiamine defic: blood thiamine (160mmol/L or CSF:serum >1.
- Sulphur tox: rumen H2S, sulfur content of feed and water
- Lead tox: blood or tissue lead, or if chronic and blood Pb no measure RBC δ‐aminolevulinic acid dehydratase; RBCs may show basophilic stippling.
11
Q
Describe necropsy findings in ruminants with PEM.
A
- Gross lesions: brain swelling with gyral flattening and coning of the cerebellum due to herniation into the foramen magnum, slight yellowish discoloration of the affected cortical tissue, autofluorescent bands of necrotic cerebral cortex when viewed with ultraviolet illumination –> macroscopically evident cavitation of cerebrocortical tissue. - Histo: necrosis of cerebrocortical neurons; neurons are shrunken and have homogeneous, eosinophilic cytoplasm, nuclei are pyknotic, faded, or absent, vessel cells undergo hypertrophy and hyperplasia; later stages –> cortical tissue undergoes cavitation as macrophages infiltrate and necrotic tissue is removed.
12
Q
Outline treatment options for PEM in ruminants.
A
- Thiamine: 10mg/kg IV q6h.
- Diuretics: 20% mannitol.
- Dexamethsone: 1-2mg/kg IV.
- Chelation therapy for Pb: EDTA IV, oral MgSO4 forms insoluble lead sulphides.
- IVFT as needed.
13
Q
Describe the rabies virus.
A
- Family: Rhabdoviridae; bullet-shaped viruses.
- Genus: Lyssavirus.
- Non-segmented, negative-stranded RNA virus.
14
Q
Describe transmission and incidence of rabies in the US.
A
- Distinct strains in raccoons (most common), skunk, bat, coyote, fox, canine.
- Transmission by exposure to saliva containing rabies virus (bite or non-bite); possible all warm-blooded animals.
- US 2012 cases: 5,669 wildlife, 115 cattle, 47 equids, 13 small ruminants, 1 human.
15
Q
Describe clinical manifestations of rabies in cattle.
A
- Multiple forms: dumb, paralytic, furious; not mutually exclusive.
- Rapidly progressive and uniformly fatal.
- Odontopharyngeal paralysis.
- Ptyalism.
- Hindlimb ataxia.
- Perineal analgesia.
- Yawning.
- Tenesmus.
- Hyperaesthesia.
- Paraphimosis.
- Hypersexuality.
16
Q
Describe the pathophysiology of rabies in ruminants.
A
- Ruminant bitten by infected animal.
- Virus uptake into peripheral nerves.
- Retrograde axoplasmic flow to the CNS.
- Incubation for 30-90 days.
- Virus replicates then invades innervated sites (salivary glands and nasal planum).
- Behaviour change enhances perpetuation.
- Shedding before clinical signs in possible.
- Causes a non-suppurative encephalitis.
17
Q
Describe diagnosis of rabies in infected ruminants.
A
- Examine whole brain.
- Histology: non-suppurative encephalitis; negri bodies are pathognomonic lesion but not seen in all cases.
- Fluorescent antibody test on brain tissue; highly specific; gold standard by public health departments.
- Notifiable!!
18
Q
What should be done with livestock potentially exposed to a rabid animal?
A
- Unvaccinated livestock: slaughter or sacrifice immediately:
- If within 7 days post‐bite: ok to eat cooked meat.
- Federal inspectors will reject if within 8 mo of known
exposure - Unvaccinated livestock, owner unwilling to slaughter: keep under close observation for 6 months.
- Currently vaccinated livestock (reg for cattle and sheep): revaccinate immediately and 45 day quarantine.
19
Q
What is the aetiologic agent of Bovine Spongiform Encephalopathy (BSE)?
A
- Transmissible spongiform encephalopathy of cattle.
- A prion i.e. infectious protein that replicates without the need for nucleic acid.
- Induces conformation change in normal cell membrane protein (PrPc) to form the abnormal prion (PrP-BSE).
20
Q
Describe the pathophysiology of BSE.
A
- Long incubation period; CSx most in 4-6yo cattle therefore higher incidence in dairy than beef breeds.
- Ingested in cattle by-products e.g. bone meal.
- Propogates in distal ileum, moves through GIT-associated lymphoid tissue to peripheral nerves –> brain, optic nerve, cervical, thoracic and trigeminal ganglia, facial and sciatic nerves.
- Accumulation of PrP-BSE in the CNS –> progressive and irreversible neuro dysfunction (exact mech unknown).
21
Q
List the clinical signs of BSE.
A
- Early subtle behaviour changes may be missed.
- Apart from herdmates.
- Apprehensive, fearful.
- Unprovoked aggression.
- Hyperaesthesia.
- Headshaking.
- Ptyalism.
- Head rubbing.
- Muscle fasciculations.
- Excessive vocalisations.
- Freq/repetitive head tossing, licking nostrils, yawning, flehmen, head butting and restlessness.
- Relative bradycardia given level of excitement.
- Wt loss and dec mild prod.
- Ataxia and tremors.
- Recumbency.
22
Q
Outline diagnosis of BSE in cattle.
A
- No in vivo test, only post-mortem.
- Histo: neuronal degeneration and intraneuronal vacuolation in specific brain areas; obex of medulla.
- Tests to ID prion in brain or SC tissue: Western blot, paraffin-embedded tissue blot, ELISAs.
